Impaired osteoinduction in a rat model for chronic alcohol abuse

Trevisiol, C.H.; Turner, Russell T.; Pfaff, Jilleen E.; Hunter, J.C.; Menagh, Philip J; Hardin, Karin; Ho, Emily; Iwaniec, Urszula T.

doi:10.1016/j.bone.2007.04.189

Cited by 50 publications

(45 citation statements)

References 34 publications

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“…Animal studies also indicated decreased osteogenesis and bone volume after long-term alcohol consumption [9, 10]. Human bone mesenchymal stem cells (hBMSCs) are regarded as the main source of self-renewal and regeneration of bone tissue [11-13], whereas recent studies demonstrated that ethanol treatment could impair the osteogenic differentiation of hBMSCs [2, 14].…”

Section: Introductionmentioning

confidence: 99%

The Protective Effect of Cordycepin On Alcohol-Induced Osteonecrosis of the Femoral Head

Chen¹,

Zhu²,

Xu³

et al. 2017

Cell Physiol Biochem

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Background: Alcohol abuse is known to be a leading risk factor for atraumatic osteonecrosis of the femoral head (ONFH), in which the suppression of osteogenesis plays a critical role. Cordycepin benefits bone metabolism; however, there has been no study to determine its effect on osteonecrosis. Methods: Human bone mesenchymal stem cells (hBMSCs) were identified by multi-lineage differentiation. Alkaline phosphatase (ALP) activity, RT-PCR, western blots, immunofluorescent assay and Alizarin red staining of BMSCs were evaluated. A rat model of alcohol-induced ONFH was established to investigate the protective role of cordycepin against ethanol. Hematoxylin & eosin (H&E) staining and micro-computerized tomography (micro-CT) were performed to observe ONFH. Apoptosis was assessed by TdT-mediated dUTP nick end labeling (TUNEL). Immunohistochemical staining was carried out to detect OCN and COL1. Results: Ethanol significantly suppressed ALP activity, decreased gene expression of OCN and BMP2, lowered levels of RUNX2 protein, and reduced immunofluorescence staining of OCN and COL1 and calcium formation of hBMSCs. However, these inhibitory effects were attenuated by cordycepin co-treatment at concentrations of 1 and 10 µg/mL Moreover, it was revealed that the osteo-protective effect of cordycepin was associated with modulation of the Wnt/β-catenin pathway. In vivo, by micro-CT, TUNEL and immunohistochemical staining of OCN and COL1, we found that cordycepin administration prevented alcohol-induced ONFH. Conclusion: Cordycepin treatment to enhance osteogenesis may be considered a potential therapeutic approach to prevent the development of alcohol-induced ONFH.

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Section: Introductionmentioning

confidence: 99%

The Protective Effect of Cordycepin On Alcohol-Induced Osteonecrosis of the Femoral Head

Chen¹,

Zhu²,

Xu³

et al. 2017

Cell Physiol Biochem

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“…Reductions in cortical thickness and trabecular bone volume have been described in rats with 36% ethanol diets (BAC= 150-210 mg/dL) [27,40] while bone atrophy, thinning of both the trabeculae and cortical bone, and increased cortical porosity have been found in Sake-fed mice (16% ethanol for 472 days) [39]. Similar data on decreased Tb.N, Tb.Th, connective density, and decreased cancellous bone volume per total tissue volume (BV/TV) were reported in rats after 35% ethanol liquid diet treatments [41,42] (Fig. 1).…”

Section: Microarchitecturementioning

confidence: 99%

Alcohol and bone: review of dose effects and mechanisms

et al. 2011

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Alcohol is widely consumed across the world. It is consumed in both social and cultural settings. Until recently, two types of alcohol consumption were recognized: heavy chronic alcohol consumption or light consumption. Today, there is a new pattern of consumption among teenagers and young adults namely: binge drinking. Heavy alcohol consumption is detrimental to many organs and tissues, including bones, and is known to induce secondary osteoporosis. Some studies, however, have reported benefits from light alcohol consumption on bone parameters. To date, little is known regarding the effects of binge drinking on bone health. Here, we review the effects of three different means of alcohol consumption: light, heavy, and binge drinking. We also review the detailed literature on the different mechanisms by which alcohol intake may decrease bone mass and strength. The effects of alcohol on bone are thought to be both direct and indirect. The decrease in bone mass and strength following alcohol consumption is mainly due to a bone remodeling imbalance, with a predominant decrease in bone formation. Recent studies, however, have reported new mechanisms by which alcohol may act on bone remodeling, including osteocyte apoptosis, oxidative stress, and Wnt signalling pathway modulation. The roles of reduced total fat mass, increased lipid content in bone marrow, and a hypoleptinemia are also discussed.

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“…Used clinically in orthopedic practice to augment bone formation during fracture repair, osteoinduction is an ideal method to investigate the effect of alcohol on mineralization because experiments can be designed in which bone is not present until introduction of alcohol into the diet. In our studies, described elsewhere in detail (Trevisiol et al 2007), subcutaneously implanted demineralized allogeneic bone matrix cylinders were used to model osteoinduction. Demineralized allogeneic bone matrix cylinders, prepared from femurs and tibiae of rats fed a normal diet, were implanted into sexually mature male rats adapted to alcohol (ethanol contributed 35% of caloric intake) or control liquid diets.…”

Section: Effects Of Alcohol On the Skeleton In Growing Ratsmentioning

confidence: 99%